subject:(HMOX1)

University of Helsinki

1. Lim, Nancy. The Role of Heme Oxygenase 1 Gene Promoter Variant in Shaping the Clinical Phenotype of Carotid Artery Disease.

Degree: Medicinska fakulteten, 2017, University of Helsinki

URL: http://hdl.handle.net/10138/228717

► Background: Atherosclerosis is a common pathological process in arteries causing significant morbidity and mortality due to stroke and myocardial infarction. The progression of atherosclerosis is… (more)

▼ Background: Atherosclerosis is a common pathological process in arteries causing significant morbidity and mortality due to stroke and myocardial infarction. The progression of atherosclerosis is affected by both genes and external factors that interactively initiate and advance the pathological cascade. Heme oxygenase 1 (HO1) is a protein that degrades toxic heme and thereby plays a role in maintaining normal vascular function. The expression of the heme oxygenase 1 gene (HMOX1) is affected by a (GT)n polymorphism in its promoter area; short (GT)n alleles associate with higher HO1 expression in cell culture studies and are hypothesized to protect vessel wall from hemi-related oxidative damage. Objective: Our research group has previously found that patients that have suffered stroke due to atherosclerotic carotid stenosis show high expression of HMOX1 in their carotid plaques (CPs). The aim of this thesis was to investigate whether this finding is explained by the HMOX1 (GT)n promoter polymorphism, i.e. if the promoter polymorphism is associated to symptomatic carotid disease. Methods: HMOX1 promoter (GT)n polymorphism was genotyped in carotid stenosis patients (HeCES n=92) and population controls (Health 2000 Survey, n=964). HMOX1 mRNA and protein levels were measured from CPs by qRT-PCR and ELISA, respectively. Results: HMOX1 promoter (GT)n alleles in the Finnish population ranged between 20 and 40 repeats, where (GT)30 was the most common allele with a population frequency of 46.6%. When comparing carotid stenosis patients to controls, statistically significant association between a lack of short alleles (< (GT)30) and symptomatic carotid disease was not found (p=0.214). Whereas, carotid stenosis patients with an ulcerative plaque lacked significantly more often a short allele at the HMOX1 promoter variant (p=0.006). However, we did not find correlation between promoter genotypes and HMOX1 mRNA or protein levels in the CPs. Conclusions: Our results support the protective role of short HMOX1 promoter (GT)n variants against symptomatic carotid artery disease (CaD).

Subjects/Keywords: stroke; atherosclerosis; carotid artery disease; HMOX1; HMOX1 promoter variants; HO1; Molecular neurology

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Lim, N. (2017). The Role of Heme Oxygenase 1 Gene Promoter Variant in Shaping the Clinical Phenotype of Carotid Artery Disease. (Masters Thesis). University of Helsinki. Retrieved from http://hdl.handle.net/10138/228717

Chicago Manual of Style (16^th Edition):

Lim, Nancy. “The Role of Heme Oxygenase 1 Gene Promoter Variant in Shaping the Clinical Phenotype of Carotid Artery Disease.” 2017. Masters Thesis, University of Helsinki. Accessed January 20, 2021. http://hdl.handle.net/10138/228717.

MLA Handbook (7^th Edition):

Lim, Nancy. “The Role of Heme Oxygenase 1 Gene Promoter Variant in Shaping the Clinical Phenotype of Carotid Artery Disease.” 2017. Web. 20 Jan 2021.

Vancouver:

Lim N. The Role of Heme Oxygenase 1 Gene Promoter Variant in Shaping the Clinical Phenotype of Carotid Artery Disease. [Internet] [Masters thesis]. University of Helsinki; 2017. [cited 2021 Jan 20]. Available from: http://hdl.handle.net/10138/228717.

Council of Science Editors:

Lim N. The Role of Heme Oxygenase 1 Gene Promoter Variant in Shaping the Clinical Phenotype of Carotid Artery Disease. [Masters Thesis]. University of Helsinki; 2017. Available from: http://hdl.handle.net/10138/228717

University of Iowa

2. Boylston, Jennifer A. FHIT inactivation combined with cigarette smoke enhances the oxidative stress response.

Degree: PhD, Molecular and Cellular Biology, 2013, University of Iowa

URL: https://ir.uiowa.edu/etd/1295

► The FHIT gene is located on the most fragile site in the human genome. FHIT gene deletions are among the earliest and most frequent… (more)

Subjects/Keywords: Bach1; Bronchial Epithelial Cells; Cigarette Smoke; Fhit; Hmox1; Oxidative Stress; Cell Biology

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Boylston, J. A. (2013). FHIT inactivation combined with cigarette smoke enhances the oxidative stress response. (Doctoral Dissertation). University of Iowa. Retrieved from https://ir.uiowa.edu/etd/1295

Chicago Manual of Style (16^th Edition):

Boylston, Jennifer A. “FHIT inactivation combined with cigarette smoke enhances the oxidative stress response.” 2013. Doctoral Dissertation, University of Iowa. Accessed January 20, 2021. https://ir.uiowa.edu/etd/1295.

MLA Handbook (7^th Edition):

Boylston, Jennifer A. “FHIT inactivation combined with cigarette smoke enhances the oxidative stress response.” 2013. Web. 20 Jan 2021.

Vancouver:

Boylston JA. FHIT inactivation combined with cigarette smoke enhances the oxidative stress response. [Internet] [Doctoral dissertation]. University of Iowa; 2013. [cited 2021 Jan 20]. Available from: https://ir.uiowa.edu/etd/1295.

Council of Science Editors:

Boylston JA. FHIT inactivation combined with cigarette smoke enhances the oxidative stress response. [Doctoral Dissertation]. University of Iowa; 2013. Available from: https://ir.uiowa.edu/etd/1295

University of Gothenburg / Göteborgs Universitet

3. Andersson, Heléne. Reactive gliosis in the injured brain: The effect of cell communication and Nrf2-mediated cellular defence.

Degree: 2011, University of Gothenburg / Göteborgs Universitet

URL: http://hdl.handle.net/2077/23937

► Stroke and other brain injuries trigger an extensive glial cell response referred to as reactive gliosis. Reactive gliosis is characterized by hypertrophic and proliferating astrocytes,… (more)

▼ Stroke and other brain injuries trigger an extensive glial cell response referred to as reactive gliosis. Reactive gliosis is characterized by hypertrophic and proliferating astrocytes, proliferating microglia and NG2-positive cells, which eventually form a bordering glial scar around the damaged area. Although reactive gliosis may protect the injured brain initially, the resulting glial scar inhibits neuronal regeneration. This thesis focuses on the role of intercellular communication and endogenous oxidative defence systems on reactive gliosis after injury. Neural cells frequently utilize gap junction channels to transport molecules between cells. We hypothesised that blocking gap junction communication would limit reactive gliosis. Two different gap junction channel blockers, octanol and carbenoxolone, were given to rats 30 min before a minor traumatic brain injury. Two days after injury, octanol decreased the extent of reactive astrocytes and NG2-positive cells, and reduced the number of reactive microglia around the wound. Carbonoxolone did not affect reactive astrocytes, but both octanol and carbenoxolone significantly decreased cell proliferation. Thus, blocking gap junction communication may attenuate the progression of reactive gliosis. Astrocytes play an essential role in antioxidant defence, much of which is regulated by the transcription factor nuclear factor (erythroid-derived 2)-like 2 (Nrf2). Nrf2 is activated by xenobiotics like sulforaphane which provides long-term protection against radical damage, even though sulforaphane is cleared from the body within a few hours. We hypothesized that this brief sulforaphane stimulation would be sufficient to induce prolonged Nrf2-induced gene expression. In primary rat astrocyte cultures, brief exposure to sulforaphane increased Nrf2-dependent gene expression; mRNA and protein levels were elevated for up to 24 h and 48 h respectively. Moreover Nrf2-dependent mRNA and proteins accumulated after repeated exposure and sulforaphane-stimulated astrocytes were more resistant to oxidative damage. Thus, stimulation of the Nrf2 pathway with sulforaphane results in prolonged elevation of endogenous antioxidants. We further hypothesised that sulforaphane-induced Nrf2 stimulation would modify stroke outcome when given after permanent focal ischaemia. Sulforaphane (a single dose or repeated dose starting 15 min after injury) did not significantly affect motor-function, infarct volume, proliferation, or glial cell activation 1 and 3 days after photothrombosis in mice. Thus, sulforaphane does not provide neuroprotection in the photothrombotic stroke model in mice when given 15 min after stroke onset. In summary, this thesis describes the kinetics of Nrf2-mediated gene expression in cultured astrocytes, and the role of intercellular communication and Nrf2 activation on aspects of reactive gliosis after brain injury.

Subjects/Keywords: Keywords: astrocyte; gap junction; Hmox1; microglia; Nrf2; Nqo1; oxidative stress; reactive gliosis

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APA (6^th Edition):

Andersson, H. (2011). Reactive gliosis in the injured brain: The effect of cell communication and Nrf2-mediated cellular defence. (Thesis). University of Gothenburg / Göteborgs Universitet. Retrieved from http://hdl.handle.net/2077/23937

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Andersson, Heléne. “Reactive gliosis in the injured brain: The effect of cell communication and Nrf2-mediated cellular defence.” 2011. Thesis, University of Gothenburg / Göteborgs Universitet. Accessed January 20, 2021. http://hdl.handle.net/2077/23937.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Andersson, Heléne. “Reactive gliosis in the injured brain: The effect of cell communication and Nrf2-mediated cellular defence.” 2011. Web. 20 Jan 2021.

Vancouver:

Andersson H. Reactive gliosis in the injured brain: The effect of cell communication and Nrf2-mediated cellular defence. [Internet] [Thesis]. University of Gothenburg / Göteborgs Universitet; 2011. [cited 2021 Jan 20]. Available from: http://hdl.handle.net/2077/23937.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Andersson H. Reactive gliosis in the injured brain: The effect of cell communication and Nrf2-mediated cellular defence. [Thesis]. University of Gothenburg / Göteborgs Universitet; 2011. Available from: http://hdl.handle.net/2077/23937

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

The Ohio State University

4. Ferguson, Jeanette M. An examination of genetic polymorphisms in the enzyme heme oxygenase-1 and their relationship to cardiovascular disease.

Degree: PhD, Pathology, 2005, The Ohio State University

URL: http://rave.ohiolink.edu/etdc/view?acc_num=osu1124123173

► Heme oxygenase-1 (HO-1) plays a critical role in protecting the cardiovascular system from the damaging effects of oxidative stress. The anti-inflammatory, antioxidant, antiproliferative and… (more)

▼ Heme oxygenase-1 (HO-1) plays a critical role in protecting the cardiovascular system from the damaging effects of oxidative stress. The anti-inflammatory, antioxidant, antiproliferative and vasodilatory effects of its reaction products (carbon monoxide, free ferrous iron, and bilirubin) mediate cardiovascular protection. Two promoter polymorphisms found in HMOX1, the gene encoding HO-1, are reported to have contrasting effects on gene transcription. The A allele of the single nucleotide polymorphism (SNP) located at base −413 has been shown to increase transcriptional activity, while a (GT)n microsatellite promoter polymorphism has been shown to decrease HMOX1 transcription when the GT repeat number exceeds 25. These polymorphisms have been associated with cardiovascular disease, and have different frequency distributions based upon ethnicity. The main goal of the experiments in this dissertation was to examine the relationship between the HMOX1 promoter polymorphisms and cardiovascular disease, while placing special emphasis on the African American ethnic group. Genotyping of the polymorphisms was performed by sequence analysis of the HMOX1 promoter. The microsatellite allele was classified as large (L) if the GT repeat was < 26 and small (S) if the GT repeat was < 26. The HMOX1 SNP-413 was genotyped according to the bases present at position −413 of the sequences. In general, the African American subjects were significantly associated with the large repeat microsatellite polymorphism and the T allele of the SNP-413. The Caucasian subjects were significantly associated with the small repeat microsatellite polymorphism and the A allele of the SNP-413. The L microsatellite allele and A SNP-413 allele was the most frequent allele combination seen in all subjects. Coronary artery disease was significantly associated with the LL microsatellite genotype in African Americans and the AA SNP-413 genotype in Caucasians. Congestive heart failure was significantly associated with the LL microsatellite genotype and TT SNP-413 genotype in African Americans. The author concludes that the large microsatellite polymorphism of HMOX1 is associated with cardiovascular disease in the African American population, and these subjects are possibly more susceptible to diseases resulting from oxidative stress due to deficient HO-1 activity. Advisors/Committee Members: Binkley, Philip (Advisor).

Subjects/Keywords: Heme Oxygenase-1; HMOX1 Microsatellite Polymorphism; HMOX1 SNP-413; Cardiovascular Disease; Genetic Polymorphisms in African Americans

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Ferguson, J. M. (2005). An examination of genetic polymorphisms in the enzyme heme oxygenase-1 and their relationship to cardiovascular disease. (Doctoral Dissertation). The Ohio State University. Retrieved from http://rave.ohiolink.edu/etdc/view?acc_num=osu1124123173

Chicago Manual of Style (16^th Edition):

Ferguson, Jeanette M. “An examination of genetic polymorphisms in the enzyme heme oxygenase-1 and their relationship to cardiovascular disease.” 2005. Doctoral Dissertation, The Ohio State University. Accessed January 20, 2021. http://rave.ohiolink.edu/etdc/view?acc_num=osu1124123173.

MLA Handbook (7^th Edition):

Ferguson, Jeanette M. “An examination of genetic polymorphisms in the enzyme heme oxygenase-1 and their relationship to cardiovascular disease.” 2005. Web. 20 Jan 2021.

Vancouver:

Ferguson JM. An examination of genetic polymorphisms in the enzyme heme oxygenase-1 and their relationship to cardiovascular disease. [Internet] [Doctoral dissertation]. The Ohio State University; 2005. [cited 2021 Jan 20]. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=osu1124123173.

Council of Science Editors:

Ferguson JM. An examination of genetic polymorphisms in the enzyme heme oxygenase-1 and their relationship to cardiovascular disease. [Doctoral Dissertation]. The Ohio State University; 2005. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=osu1124123173

University of Oulu

5. Lämsä, V. (Virpi). Regulation of murine hepatic Cytochrome P450 2a5 expression by transcription factor Nuclear factor (erythroid-derived 2)-like 2.

Degree: 2012, University of Oulu

URL: http://urn.fi/urn:isbn:9789514299278

►

Abstract The hepatic inducible Cytochrome P450s (CYPs) generally prime xenobiotics for elimination. Murine CYP2A5 and human CYP2A6 share similar xenobiotic substrates and some regulatory features.… (more)

▼

Abstract The hepatic inducible Cytochrome P450s (CYPs) generally prime xenobiotics for elimination. Murine CYP2A5 and human CYP2A6 share similar xenobiotic substrates and some regulatory features. Recently, they were shown to oxidize bilirubin, a byproduct of heme catabolism and a dose-dependent anti- or pro-oxidant, to biliverdin. In this study, the putative role of the redox-sensitive, cytoprotective transcription factor Nuclear factor (erythroid-derived 2)-like 2 (Nrf2) in the regulation of hepatic Cyp2a5 expression and induction under diverse hepatotoxic conditions and altered heme homeostasis was characterized. The coordination of Cyp2a5 and the Nrf2 target gene Heme oxygenase-1 (Hmox1), which determines bilirubin formation from heme, responses to heavy metals and modulators of heme homeostasis, was studied in cultured wildtype and Nrf2(-/-) mouse primary hepatocytes. Nrf2 was essential for the basal hepatic expression of CYP2A5 in the endoplasmic reticulum (ER) and mitochondria, as well as for its induction by cadmium, lead, methyl mercury and phenethyl isothiocyanate. A functional Nrf2 binding antioxidant response element (ARE) about -2.4 kilobases upstream of the Cyp2a5 transcriptional start site was identified. In contrast to Hmox1, a target of BTB and CNC homology 1 (Bach)-mediated repression via AREs, the regulation of Cyp2a5 did not clearly involve Bach1. Excessive heme induced mainly ER-localized CYP2A5 via Nrf2, which was limited by the Nrf2-independent HMOX1 induction. In heme synthesis blockades, CYP2A5 was enhanced via Nrf2 and additional factors, such as the peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α). The typical CYP2A5 inducers phenobarbital, dibutyryl-cyclic adenosine monophosphate (db-cAMP) and PGC-1α enhance heme synthesis; CYP2A5 was induced via Nrf2 in acute but not chronic phenobarbital exposure without a clear connection to heme, while the responses to db-cAMP and PGC-1α were sensitized in the absence of Nrf2. This suggests novel crosstalk between Nrf2 and PGC-1α. In this study, Cyp2a5 was identified as a sensitive indicator of hepatic Nrf2 pathway activation that could be used, e.g. for in vitro screening of drug candidate hepatotoxicity. The similar subcellular localization and coordination of CYP2A5 and HMOX1 expression in altered heme metabolism support the postulated role for CYP2A5 in bilirubin homeostasis.

Tiivistelmä Vierasaineet stimuloivat maksan Sytokromi P450 (CYP)-entsyymejä, mikä yleensä lisää niiden eliminaatiota. Hiiren CYP2A5 ja ihmisen CYP2A6 ovat lähisukua katalyyttisten ja osin säätelyllisten yhteneväisyyksiensä puolesta. Vastikään niiden osoitettiin katalysoivan hemin hajoamistuotteen, bilirubiinin hapettumista biliverdiiniksi, mikä saattaisi säädellä sen annosriippuvaisia vaikutuksia antioksidanttina ja oksidanttina. Työssä tutkittiin solustressiä aistivan, suojaavan transkriptiotekijän Nrf2 osuutta Cyp2a5-geenin aktivaatiossa maksatoksisissa olosuhteissa ja hemimetabolian muutoksissa. Cyp2a5:n ja…

Advisors/Committee Members: Hakkola, J. (Jukka).

Subjects/Keywords: Bach1; CYP2A5; HMOX1; Nrf2; PGC-1α; heavy metals; heme homeostasis; hepatotoxicity; liver; redox homeostasis; transcriptional regulation; xenobiotic metabolism; aineenvaihdunta; antioksidantit; entsyymit; geeniekspressio; geenitutkimus; hapettuminen; maksa; markkerit; mitokondriot; oksidantit; raskasmetallit; sytokromit; toksikologia; transkriptio; vierasaineet

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Lämsä, V. (. (2012). Regulation of murine hepatic Cytochrome P450 2a5 expression by transcription factor Nuclear factor (erythroid-derived 2)-like 2. (Doctoral Dissertation). University of Oulu. Retrieved from http://urn.fi/urn:isbn:9789514299278

Chicago Manual of Style (16^th Edition):

Lämsä, V (Virpi). “Regulation of murine hepatic Cytochrome P450 2a5 expression by transcription factor Nuclear factor (erythroid-derived 2)-like 2.” 2012. Doctoral Dissertation, University of Oulu. Accessed January 20, 2021. http://urn.fi/urn:isbn:9789514299278.

MLA Handbook (7^th Edition):

Lämsä, V (Virpi). “Regulation of murine hepatic Cytochrome P450 2a5 expression by transcription factor Nuclear factor (erythroid-derived 2)-like 2.” 2012. Web. 20 Jan 2021.

Vancouver:

Lämsä V(. Regulation of murine hepatic Cytochrome P450 2a5 expression by transcription factor Nuclear factor (erythroid-derived 2)-like 2. [Internet] [Doctoral dissertation]. University of Oulu; 2012. [cited 2021 Jan 20]. Available from: http://urn.fi/urn:isbn:9789514299278.

Council of Science Editors:

Lämsä V(. Regulation of murine hepatic Cytochrome P450 2a5 expression by transcription factor Nuclear factor (erythroid-derived 2)-like 2. [Doctoral Dissertation]. University of Oulu; 2012. Available from: http://urn.fi/urn:isbn:9789514299278

University of Cincinnati

6. MA, CI, Miss. THE TRANSCRIPTION FACTOR BTB AND CNC HOMOLOG 1 IN THE REGULATION OF CELL DIFFERENTIATION AND ORGANOGENESIS.

Degree: MS, Medicine : Toxicology (Environmental Health), 2007, University of Cincinnati

URL: http://rave.ohiolink.edu/etdc/view?acc_num=ucin1185995222

► BACH1 (BTB and CNC homolog 1) is a transcription factor that belongs to the CNC (cap'n'collar)-type bZip (basic region leucine zipper) transcription factor family. A… (more)

Subjects/Keywords: Health Sciences, Toxicology; BACH1; HMOX1; NQO1; transcription factor; stably-transfection; real-time PCR; western blotting

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

MA, CI, M. (2007). THE TRANSCRIPTION FACTOR BTB AND CNC HOMOLOG 1 IN THE REGULATION OF CELL DIFFERENTIATION AND ORGANOGENESIS. (Masters Thesis). University of Cincinnati. Retrieved from http://rave.ohiolink.edu/etdc/view?acc_num=ucin1185995222

Chicago Manual of Style (16^th Edition):

MA, CI, Miss. “THE TRANSCRIPTION FACTOR BTB AND CNC HOMOLOG 1 IN THE REGULATION OF CELL DIFFERENTIATION AND ORGANOGENESIS.” 2007. Masters Thesis, University of Cincinnati. Accessed January 20, 2021. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1185995222.

MLA Handbook (7^th Edition):

MA, CI, Miss. “THE TRANSCRIPTION FACTOR BTB AND CNC HOMOLOG 1 IN THE REGULATION OF CELL DIFFERENTIATION AND ORGANOGENESIS.” 2007. Web. 20 Jan 2021.

Vancouver:

MA, CI M. THE TRANSCRIPTION FACTOR BTB AND CNC HOMOLOG 1 IN THE REGULATION OF CELL DIFFERENTIATION AND ORGANOGENESIS. [Internet] [Masters thesis]. University of Cincinnati; 2007. [cited 2021 Jan 20]. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=ucin1185995222.

Council of Science Editors:

MA, CI M. THE TRANSCRIPTION FACTOR BTB AND CNC HOMOLOG 1 IN THE REGULATION OF CELL DIFFERENTIATION AND ORGANOGENESIS. [Masters Thesis]. University of Cincinnati; 2007. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=ucin1185995222

University of Queensland

7. Hu, Hao. Transcriptional regulation of human stress responsive cytochrome P450 2A6 (CYP2A6) by p53.

Degree: School of Medicine, 2016, University of Queensland

URL: http://espace.library.uq.edu.au/view/UQ:405743

Subjects/Keywords: Cytochrome P450 2A6 (CYP2A6); Bilirubin (BR); Haem oxygenase1 (HMOX1); Benzo[α]pyrene (BaP); Nuclear factor erythroid 2-like 2 (Nrf-2); Tumour suppressor p53; Constitutive androstane receptor (CAR); CEBP α; Octamer-1 (Oct-1); Hepatocyte nuclear factor-4α (HNF-4α); 060107 Enzymes; 060111 Signal Transduction; 060199 Biochemistry and Cell Biology not elsewhere classified

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Hu, H. (2016). Transcriptional regulation of human stress responsive cytochrome P450 2A6 (CYP2A6) by p53. (Thesis). University of Queensland. Retrieved from http://espace.library.uq.edu.au/view/UQ:405743

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Hu, Hao. “Transcriptional regulation of human stress responsive cytochrome P450 2A6 (CYP2A6) by p53.” 2016. Thesis, University of Queensland. Accessed January 20, 2021. http://espace.library.uq.edu.au/view/UQ:405743.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Hu, Hao. “Transcriptional regulation of human stress responsive cytochrome P450 2A6 (CYP2A6) by p53.” 2016. Web. 20 Jan 2021.

Vancouver:

Hu H. Transcriptional regulation of human stress responsive cytochrome P450 2A6 (CYP2A6) by p53. [Internet] [Thesis]. University of Queensland; 2016. [cited 2021 Jan 20]. Available from: http://espace.library.uq.edu.au/view/UQ:405743.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Hu H. Transcriptional regulation of human stress responsive cytochrome P450 2A6 (CYP2A6) by p53. [Thesis]. University of Queensland; 2016. Available from: http://espace.library.uq.edu.au/view/UQ:405743

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

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